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. 2021 Jul 21;40(34):5253–5261. doi: 10.1038/s41388-021-01946-8

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — The tumor microenvironment (TME) may inhibit dendritic cell (DC) functions, abrogating DCs’ ability to promote T cell responses. Tumor cells often upregulate the expression of CD47, which may inhibit DC presentation of antigens to T cells. In addition, the accumulated lipid and metabolites within the TME exhibit similar negative effects on DC antigen presentation. Moreover, the elevated concentrations of TGF-β and Wnt, as well as LXRα, promote DC migration to the tumor but block migration to the lymph nodes. Furthermore, the TME is rich in cytokines IL-6, IL-10, and TGF-β, as well as tumor-derived VEGF. These molecules inhibit DC maturation, altering their ability to initiate a T cell response.